Objectives The aim of this study was to identify the determinants of plaque structural stress (PSS) and the relationship between PSS and plaques with rupture.

Background Plaque rupture is the most common cause of myocardial infarction, occurring particularly in higher risk lesions such as fibroatheromas. However, prospective intravascular ultrasound–virtual histology studies indicate that <10% higher risk plaques cause clinical events over 3 years, indicating that other factors also determine plaque rupture. Plaque rupture occurs when PSS exceeds its mechanical strength; however, the determinants of PSS and its association with plaques with proven rupture are not known.

Methods We analyzed plaque structure and composition in 4,053 virtual histology intravascular ultrasound frames from 32 fibroatheromas with rupture from the intravascular ultrasound–virtual histology in Vulnerable Atherosclerosis study and 32 fibroatheromas without rupture on optical coherence tomography from a stable angina cohort. Mechanical loading in the periluminal region was estimated by calculating maximum principal PSS by finite element analysis.

Results PSS increased with increasing lumen area (r = 0.46; p = 0.001), lumen eccentricity (r = 0.32; p = 0.001), and necrotic core ≥10% (r = 0.12; p = 0.001), but reduced when dense calcium was ≥10% (r = −0.12; p = 0.001). Ruptured fibroatheromas showed higher PSS (133 kPa [quartiles 1 to 3: 90 to 191 kPa] vs. 104 kPa [quartiles 1 to 3: 75 to 142 kPa]; p = 0.002) and variation in PSS (55 kPa [quartiles 1 to 3: 37 to 75 kPa] vs. 43 kPa [quartiles 1 to 3: 34 to 59 kPa]; p = 0.002) than nonruptured fibroatheromas, with rupture primarily occurring either proximal or immediately adjacent to the minimal luminal area (87.5% vs. 12.5%; p = 0.001). PSS was higher in segments proximal to the rupture site (143 kPa [quartiles 1 to 3: 101 to 200 kPa] vs. 120 kPa [quartiles 1 to 3: 78 to 180 kPa]; p = 0.001) versus distal segments, associated with increased necrotic core (19.1% [quartiles 1 to 3: 11% to 29%] vs. 14.3% [quartiles 1 to 3: 8% to 23%]; p = 0.001) but reduced fibrous/fibrofatty tissue (63.6% [quartiles 1 to 3: 46% to 78%] vs. 72.7% [quartiles 1 to 3: 54% to 86%]; p = 0.001). PSS >135 kPa was a good predictor of rupture in higher risk regions.

Conclusions PSS is determined by plaque composition, plaque architecture, and lumen geometry. PSS and PSS variability are increased in plaques with rupture, particularly at proximal segments. Incorporating PSS into plaque assessment may improve identification of rupture-prone plaques.

目的本研究的目的是确定斑块结构应力 (PSS) 的决定因素以及 PSS 与斑块破裂之间的关系。

背景斑块破裂是心肌梗塞的最常见原因，尤其发生在纤维粥样硬化等高风险病变中。然而，前瞻性血管内超声-虚拟组织学研究表明，<10% 的高风险斑块会导致 3 年内的临床事件，表明其他因素也决定斑块破裂。当 PSS 超过其机械强度时，就会发生斑块破裂；然而，PSS 的决定因素及其与已证实破裂的斑块的关系尚不清楚。

方法我们分析了 4,053 个虚拟组织学血管内超声帧中的斑块结构和成分，这些帧来自脆弱动脉粥样硬化研究中血管内超声虚拟组织学中的 32 个破裂纤维粥样斑块，以及稳定型心绞痛队列中光学相干断层扫描中的 32 个未破裂纤维粥样斑块。通过有限元分析计算最大主 PSS 来估计管腔周围区域的机械载荷。

结果PSS 随着管腔面积 (r = 0.46; p = 0.001)、管腔偏心率 (r = 0.32; p = 0.001) 和坏死核心≥10% (r = 0.12; p = 0.001) 的增加而增加，但当致密钙时 PSS 降低≥10%（r = -0.12；p = 0.001）。破裂的纤维粥样斑块表现出较高的 PSS（133 kPa [四分位数 1 至 3：90 至 191 kPa] 与 104 kPa [四分位数 1 至 3：75 至 142 kPa]；p = 0.002）和 PSS 变化（55 kPa [四分位数 1 至 3：90 至 191 kPa] 3: 37 至 75 kPa] vs. 43 kPa [四分位数 1 至 3: 34 至 59 kPa]; p = 0.002) 比非破裂性纤维粥样斑块高，破裂主要发生在最小管腔区域的近端或紧邻区域（87.5% vs. 87.5%） 12.5%；p = 0.001）。与远端节段相比，靠近破裂部位的节段的 PSS 较高（143 kPa [四分位数 1 至 3：101 至 200 kPa] 与 120 kPa [四分位数 1 至 3：78 至 180 kPa]；p = 0.001），这与坏死核心增加（19.1% [四分位数 1 至 3：11% 至 29%] 对比 14.3% [四分位数 1 至 3：8% 至 23%]；p = 0.001），但纤维/纤维脂肪组织减少（63.6% [四分位数1 至 3：46% 至 78%] 对比 72.7% [四分位数 1 至 3：54% 至 86%]；p = 0.001）。PSS >135 kPa 是高风险区域破裂的良好预测指标。

结论PSS 由斑块组成、斑块结构和管腔几何形状决定。PSS 和 PSS 变异性在破裂斑块中增加，特别是在近端节段。将 PSS 纳入斑块评估可能会改善易破裂斑块的识别。